The ensuing fast rebound burst was due to T-type calcium current,

The ensuing fast rebound burst was due to T-type calcium current, as previously described. It was highly variable between cells in strength, and could

be expressed fully after short periods of hyperpolarization. In contrast, a subsequent prolonged rebound component required longer and deeper periods of hyperpolarization before it was fully established. We found using voltage-clamp and dynamic-clamp analyses that a slowly inactivating persistent sodium current fits the conductance underlying this prolonged rebound component, resulting in spike rate increases over several seconds. Overall, our results demonstrate that multiphasic DCN rebound properties could be elicited differentially by different levels of Purkinje cell activation, and thus create a rich repertoire of potential rebound dynamics in the cerebellar control of motor selleck compound timing. “
“Microglia

colonise the brain parenchyma at early stages of development and accumulate in specific regions where they participate in cell death, angiogenesis, neurogenesis and synapse elimination. A recurring feature of embryonic microglial is their association with developing axon tracts, which, together with in vitro data, supports the idea of a physiological role for microglia CHIR-99021 mw in neurite development. Yet the demonstration of this role of microglia is lacking. Here, we have studied the consequences of microglial dysfunction on the formation of the corpus callosum, the largest commissure of the mammalian brain, which shows consistent microglial accumulation during development. We studied two models of microglial dysfunction: the loss-of-function of DAP12, a key microglial-specific signalling molecule, and a model of maternal inflammation by peritoneal injection of lipopolysaccharide at embryonic day (E)15.5. We also took advantage of the Pu.1−/− mouse line, which is devoid of microglia. We performed transcriptional profiling of maternally inflamed and Dap12-mutant microglia at E17.5. The two treatments principally down-regulated genes involved in nervous system development

and function, particularly in neurite formation. We then analysed the developmental consequences of these microglial dysfunctions on the formation of the corpus callosum. We Dimethyl sulfoxide show that all three models of altered microglial activity resulted in the defasciculation of dorsal callosal axons. Our study demonstrates that microglia display a neurite-development-promoting function and are genuine actors of corpus callosum development. It further shows that microglial activation impinges on this function, thereby revealing that prenatal inflammation impairs neuronal development through a loss of trophic support. “
“Parkinson’s disease is characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN). However, whether regenerative endogenous neurogenesis is taking place in the mammalian SN of parkinsonian and non-parkinsonian brains remains of debate.

The ensuing fast rebound burst was due to T-type calcium current,

The ensuing fast rebound burst was due to T-type calcium current, as previously described. It was highly variable between cells in strength, and could

be expressed fully after short periods of hyperpolarization. In contrast, a subsequent prolonged rebound component required longer and deeper periods of hyperpolarization before it was fully established. We found using voltage-clamp and dynamic-clamp analyses that a slowly inactivating persistent sodium current fits the conductance underlying this prolonged rebound component, resulting in spike rate increases over several seconds. Overall, our results demonstrate that multiphasic DCN rebound properties could be elicited differentially by different levels of Purkinje cell activation, and thus create a rich repertoire of potential rebound dynamics in the cerebellar control of motor selleck chemicals timing. “
“Microglia

colonise the brain parenchyma at early stages of development and accumulate in specific regions where they participate in cell death, angiogenesis, neurogenesis and synapse elimination. A recurring feature of embryonic microglial is their association with developing axon tracts, which, together with in vitro data, supports the idea of a physiological role for microglia CHIR-99021 clinical trial in neurite development. Yet the demonstration of this role of microglia is lacking. Here, we have studied the consequences of microglial dysfunction on the formation of the corpus callosum, the largest commissure of the mammalian brain, which shows consistent microglial accumulation during development. We studied two models of microglial dysfunction: the loss-of-function of DAP12, a key microglial-specific signalling molecule, and a model of maternal inflammation by peritoneal injection of lipopolysaccharide at embryonic day (E)15.5. We also took advantage of the Pu.1−/− mouse line, which is devoid of microglia. We performed transcriptional profiling of maternally inflamed and Dap12-mutant microglia at E17.5. The two treatments principally down-regulated genes involved in nervous system development

and function, particularly in neurite formation. We then analysed the developmental consequences of these microglial dysfunctions on the formation of the corpus callosum. We enough show that all three models of altered microglial activity resulted in the defasciculation of dorsal callosal axons. Our study demonstrates that microglia display a neurite-development-promoting function and are genuine actors of corpus callosum development. It further shows that microglial activation impinges on this function, thereby revealing that prenatal inflammation impairs neuronal development through a loss of trophic support. “
“Parkinson’s disease is characterized by a selective loss of dopaminergic neurons in the substantia nigra (SN). However, whether regenerative endogenous neurogenesis is taking place in the mammalian SN of parkinsonian and non-parkinsonian brains remains of debate.

In all known cases, in normally growing cells, toxins form a stab

In all known cases, in normally growing cells, toxins form a stable complex with their cognate antitoxins that blocks the toxin activity. Antitoxin also functions as a repressor for individual TA operons (Gerdes et al., 2005). Under stress conditions, intrinsically unstable antitoxin is lost from the cells, releasing toxin freely and inhibiting various essential cellular functions, such as DNA replication, mRNA stability, protein synthesis, and cell division (Jiang

et al., 2002; Zhang et al., 2003; Tan et al., Venetoclax ic50 2011; Zhang & Inouye, 2011). This leads to a reversible cell growth arrest, which is implicated in the persister phenotype. The TA system is also shown to be associated with pathogenicity, programmed cell death, and biofilm formation (Pandey & Gerdes, 2005; Nariya & Inouye, 2008; Wang & Wood, 2011). Escherichia coli have two essential bacterial cytoskeletal proteins, FtsZ and MreB. FtsZ is a highly conserved GTPase and is homologous to eukaryotic cytoskeleton protein, tubulin (Mukherjee et al., 1998). It forms a ring structure at the mid-cell and functions as a scaffold for divisome, a multiprotein

complex responsible for cell division. MreB is an actin-like ATPase, essential for maintaining the typical rod shape and cell polarity in E. coli (Osborn & Rothfield, 2007). MreB is also implicated in chromosome segregation, localization of membranous organelles, and coordinating cell division with cell biosynthesis (Kruse et al., 2005; Komeili et al., 2006; Madabhushi & Marians, 2009; Domínguez-Escobar et al., 2011; selleck chemical ADP ribosylation factor Garner et al., 2011). Because both FtsZ and MreB are involved in a number of essential cellular functions, the inhibition of their functions is detrimental to the cells. For example, the inhibition of FtsZ polymerization by SulA or MinCD results in blocking the septum formation, causing the formation of filamentous cells (Mukherjee et al., 1998; Pichoff & Lutkenhaus, 2001). The inhibition of MreB by A22 [S-(3,4-dichlorobenzyl) isothiourea] leads to the loss of its rod shape and eventual cell lysis (Karczmarek et al.,

2007; Bean et al., 2009). Here, we have identified a novel TA system in E. coli genome using RASTA (Sevin & Barloy-Hubler, 2007). The putative toxin, YgfX, inhibits the cell growth and causes significant changes in the cellular morphology of E. coli. Upon induction of YgfX, the cells were first elongated and then subsequently became inflated in the middle. The YgfX toxicity was neutralized by the co-expression of YgfY, indicating that YgfY is an antitoxin of YgfX. YgfX is the first toxin of E. coli TA systems shown to be associated with membrane. We further demonstrated that YgfX physically interacts with FtsZ and MreB and inhibits their polymerization in vitro and that the C-terminal soluble domain of the YgfX is responsible for the inhibition.

1, SAS Inc, Cary, NC, USA) except MCA which was conducted with X

1, SAS Inc., Cary, NC, USA) except MCA which was conducted with XLStat 2007.5 software (Addinsoft, Paris, France). Between June 2005 and May 2009, travel outside Canada was recorded in 493 cases reported in the study area. Six of these cases reported onset dates before their departure dates, three cases reported onset dates after departure and before the minimum incubation period, and 38 cases reported onset dates after their return

dates and LDK378 concentration beyond the maximum incubation period. Thus, these 47 cases were considered as DC, leaving 446 TRC for analysis. The three most frequent diseases among TRC were Campylobacter enteritis, non-typhoidal salmonellosis, and giardiasis, accounting for three quarters of the cases (Table 1). Thirty-four cases were hospitalized; the most with salmonellosis (12 cases) or paratyphoid or typhoid fever (9 cases) (Table 1). Overall, the selleck screening library most common symptoms were diarrhea (77%), abdominal pain (58%), malaise (52%), fever (51%), nausea (44%), and headache (36%) with some variations between illnesses (Table 1). The onset date was available for 379 cases (85%)

with the following yearly distribution (from June to May the following year): 82 cases in 2005 to 2006, 117 cases in 2006 to 2007, 97 cases in 2007 to 2008, and 83 cases in 2008 to 2009. The total monthly distribution combined over 4 years ranged from 23 cases in October to 51 cases in August. No significant differences were found between years and months. Both onset and return dates were recorded in 353 cases (79%). The onset date for 204 of these cases (58%) occurred after their return date; and within the first 4 days for 75% of them (Figure 1). The other cases (148/353 or 42%) became ill while abroad, within the last 7 days prior to return for 60% of them (Figure 1). Among the cases who became ill abroad with known departure date (n = 143), the delay between

departure and onset dates had the following quartiles: 5 (Q1), 7 (median), and 20 days (Q3). Overall, 50.4% TRC were Idoxuridine male with some variations between diseases (Table 2). Age ranged from a few months to 80 years with a right skewed distribution, the quartiles being 12 (Q1), 26 (median), and 46 (Q3). The disease-specific age distribution showed potentially different patterns; cryptosporidiosis TRC were less than 40 years old, cyclosporiasis TRC over 25 years, and hepatitis A TRC under 25 years (Table 2). Among the 446 TRC, 42 (9.4%) were classified as new immigrants as a result of adoption (6 cases), refugee status (16 cases), or immigration (20 cases). Most of them were in the 5 to 14 years (23 cases) or <5-year-age groups (8 cases). Overall, the main destinations were to Latin America/Caribbean (160 cases) and Asia (134 cases), with some variations between the diseases (Table 3). Destination for cases identified as new immigrants were Asia (23 cases), Africa (12 cases), and Latin America/Caribbean (7 cases).

The authors state that they have no conflicts of interest “

The authors state that they have no conflicts of interest. “
“Compared with other infections, such as yellow fever or malaria, awareness of the potential for travelers to contract meningococcal disease is low. Global disease incidence rates, however, may be as high as 1,000/100,000 population in the “meningitis belt” of sub-Saharan Africa and are generally between 100 and 800/100,000 population during epidemics in Africa.1,2 In the United States, the annual incidence is 0.5 to 1.1/100,000 DAPT chemical structure or about 1,400 to 2,800 cases annually.3 Although the highest disease incidence is in infants, in many regions

and countries, a second peak occurs in the 14- to 25-year-old demographic. Surveillance data from 1999 to 2008 estimated the Nutlin-3a cell line highest rates of meningococcal disease incidence in the United States were in children aged 4 years and younger (∼2/100,000 population) and adolescents aged 15 to 19 years (∼1/100,000 population).4 In addition to consideration of the disease incidence, it is also important to consider the impact of meningococcal disease on the patient. Onset of meningococcal disease is often sudden and the rate of progression is unpredictable. Initial symptoms are nonspecific and can resemble those of other common

and/or benign diseases.5 Therefore, it may be difficult to identify and treat the disease quickly. Invasive disease may develop 1 to 14 days after acquisition of meningococci.6 Despite the availability of appropriate treatment and intensive enough care, up to 10% to 14% of persons in the United States and 5% to 10% of persons worldwide who contract meningococcal disease die, with a rate of ∼40%

among patients with meningococcal sepsis.1,5,7 Additionally, 11% to 19% of persons who survive meningococcal disease can suffer from permanent disabilities, including brain damage, hearing loss, limb loss, or learning disabilities.5,7 The rapid progression and devastating consequences of disease make prevention through vaccination the best option for controlling meningococcal disease in the community. For travelers, the risk of contracting invasive meningococcal disease depends on their destination, duration of travel, and behavior while at their destination. For example, Hajj pilgrims (for whom vaccination is required),8 travelers spending extended stays in areas where disease is epidemic or hyperendemic, and those having a high degree of interaction with local communities at risk are all at increased risk for contracting meningococcal disease.9 Guidance on vaccinating travelers against meningococcal disease is provided by national health authorities as well as the World Health Organization (WHO) and, in recent years, has been updated to reflect the development of multivalent meningococcal conjugate vaccines.

To assess the extent of HIVDR in the Asia-Pacific, the TREAT Asia

To assess the extent of HIVDR in the Asia-Pacific, the TREAT Asia network has developed the TREAT Asia Studies to Evaluate Resistance (TASER) programme [36]. The programme includes a monitoring protocol (TASER-M), a surveillance protocol (TASER-S) and a laboratory component, the TREAT Asia Quality Assurance Scheme (TAQAS). Patients eligible for TASER-M are those initiating first-line ART or switching to second-line ART. Objectives are to assess the prevalence and incidence of emerging HIVDR and to produce evidence-based recommendations to inform treatment guidelines. The objective of TASER-S is to evaluate the prevalence and changes in prevalence of HIVDR in treatment-naïve, recently infected HIV-positive individuals.

TAQAS is a laboratory network building capacity for the genetic analysis of clinical specimens and participating laboratories provide genotypic results for the TASER protocols. In summary, less-than-annual site-reported VL testing was associated with less Obeticholic Acid supplier favourable patient outcomes, in particular, a 35% increased risk of AIDS and death. Outcomes for patients at

sites reporting VL testing one to two times annually did not differ substantially from those of patients at sites reporting more frequent monitoring. Our findings emphasize the need to partner the expanded international access to ARVs with appropriate levels of VL diagnostic testing and to address click here the critical lack of second- and third-line treatment regimens in resource-limited settings. The TREAT Asia HIV Observational Database is part of the Asia Pacific HIV Observational Database and is an initiative of TREAT Asia, a programme of amfAR, The Foundation for AIDS Research, with support from the National Institute of Allergy and Infectious Diseases (NIAID) of the US National Institutes of Health (NIH) as part of the International Epidemiologic Databases to Evaluate AIDS (IeDEA) (grant no. U01AI069907), and from the Dutch Ministry of Foreign Affairs through a partnership with Stichting Aids Fonds. The National Centre in HIV Epidemiology and Clinical Research is funded by

the Australian Akt inhibitor Government Department of Health and Ageing, and is affiliated with the Faculty of Medicine, The University of New South Wales. The content of this publication is solely the responsibility of the authors and does not necessarily represent the official views of any of the institutions mentioned above. Potential conflicts of interest: PL Lim is an investigator on Tibotec study TMC 114-C211 (Artemis). There are no conflicts of interest to report for any of the other authors. Role of the funding source: The funding source played no role in the study design, data collection, analysis, data interpretation or writing of the report. V. Saphonn*, C.V. Mean and K. Vohith, National Center for HIV/AIDS, Dermatology & STDs, Phnom Penh, Cambodia; F.J. Zhang*, H.X. Zhao and N. Han, Beijing Ditan Hospital, Beijing, China; P.C.K. Li*† and M.P. Lee, Queen Elizabeth Hospital, Hong Kong, China; N.

Most remarkably, this study provides new data on DENV strains cir

Most remarkably, this study provides new data on DENV strains circulating in Africa, where only scarce data

are available. The role of travelers and nonendemic countries as an additional source of epidemiological data on infectious diseases, complementary to the information available from endemic countries, has been demonstrated.7–9 Samples (sera and/or viral culture supernatants) were collected by virology research laboratories of the European Network for Diagnosis of “Imported” Viral Diseases (ENIVD) or travel clinics members of the European Network on Imported Infectious Diseases Surveillance (TropNetEurop) from 2002 to 2008. Seven ENIVD laboratories participated in the study, which are all national reference laboratories. HIF inhibitor review They received samples routinely from a wide range of clinics and hospitals in the countries for dengue confirmation. Within the TropNetEurop a total of five travel selleckchem clinics participated. In these clinics, a suspected dengue case was defined as

a patient with travel history in the previous 15 days to a dengue endemic area, who presented fever plus two of the following symptoms or hematological findings: myalgia, arthralgia, headache, retro-orbital pain, malaise, rash, bleeding tendencies, positive tourniquet test, leucopoenia, or thrombocytopenia. Further details on the clinical presentations of dengue patients included have been published previously.10,11 Confirmation of acute dengue infection in those serum samples received during the study and case classification (primary or secondary infections) were carried out by molecular and serological diagnosis.12 Samples were stored at −80°C until further processing. Viral RNA was obtained using the QIAamp

Viral RNA Minikit (Qiagen, Hilden, Germany). RNA was subjected to a reverse transcriptase-polymerase chain reaction (RT-PCR) (Access One-Step RT-PCR, Abiraterone purchase Promega GmbH, Mannheim, Germany) to amplify a 445, 529, 459, and 460 bp fragment for DENV-1, DENV-2, DENV-3, and DENV-4, respectively, spanning the E/NS1 junction of the DENV genome.13 A multiplex-nested PCR was carried out, using a mix of dengue-specific oligonucleotides (Table 1). Positive samples which showed higher viral loads were also subjected to a specific DENV RT-nested PCR to amplify the complete E gene using specific primers for each DENV serotype (Table 2). The sequences of the E/NS1 fragment were obtained using the forward and the reverse primer-nested PCR mix flanking the amplification product, and the ABI Prism Dye terminator cycle sequencing ready reaction kit (Applied Biosystems, Foster City, CA, USA). A minimum number of four sequences were compiled to gain a consensus sequence. To sequence the complete E gene, different DENV serotype specific primers were used to obtain overlapping sequences (Table S1, Supporting Information). Original sequence data were first analyzed by the CHROMAS software (version 1.

Mutations in 23S rRNA gene at positions 2058 and 2059 are most co

Mutations in 23S rRNA gene at positions 2058 and 2059 are most commonly associated with macrolide resistance Venetoclax in many species including M. gallisepticum (Vester & Douthwaite, 2001; Wu et al., 2005). Not unexpectedly, M. gallisepticum mutants with the A2058G or the A2059G mutation exhibited cross-resistance to

erythromycin, tilmicosin and tylosin in this study. This finding is important as macrolides are also common drugs for the treatment of M. gallisepticum infection. In conclusion, our study showed that mutations in 23S rRNA gene were responsible for resistance to pleuromutilin antibiotics in M. gallisepticum. Some of these mutations led to cross-resistance to other classes of antibiotics including macrolides, lincosamides and phenicols. Notably, no mutations in ribosomal protein L3 were found in this study. This is the first report of pleuromutilin resistance mechanisms in Mycoplasma spp. Further study should be carried out to investigate whether clinical isolates of M. gallisepticum PF-562271 price also contain these mutations in 23S rRNA gene. If so, the cross-resistance mediated by 23S rRNA gene mutations should be considered in the treatment of M. gallisepticum

infection. We wish to thank Dr Jin Zhu (University of Canberra, Australia) for suggested revisions of the manuscript. This study was supported by a grant from the National Natural Science Foundation of China (No. 30571401) and the Program for Chang Jiang Scholars and the Innovative Research Team at the University of China (No. IRT0866). “
“Autophagy is a degradation system in which cellular Baf-A1 molecular weight components are digested via vacuoles/lysosomes, and involved in differentiation in addition to helping cells to survive starvation. The autophagic process is composed of several steps: induction of autophagy, formation of autophagosomes, transportation to vacuoles, and

degradation of autophagic bodies. To further understand autophagy in the filamentous fungus Aspergillus oryzae, we first constructed A. oryzae mutants defective for the Aoatg13, Aoatg4, and Aoatg15 genes and examined the resulting phenotypes. The ΔAoatg13 mutant developed conidiophores and conidia, although the number of conidia was decreased compared with the wild-type strain, while conidiation in the ΔAoatg4 and ΔAoatg15 mutants was not detected. The ΔAoatg15 mutants displayed a marked reduction of development of aerial hyphae. Moreover, autophagy in these mutants was examined by observation of the behavior of enhanced green fluorescent protein (EGFP)–AoAtg8.

albicans strain (Asai et al, 1999) Several enzymes of the posts

albicans strain (Asai et al., 1999). Several enzymes of the postsqualene ergosterol biosynthetic pathway require molecular oxygen, making ergosterol biosynthesis an oxygen-dependent process. When grown under aerobic conditions, S. cerevisiae is Selleck Tacrolimus able to synthesize sterols, and is unable to acquire exogenous sterols, a phenomenon known as aerobic sterol exclusion (Andreasen & Stier, 1953). Under anaerobic conditions, the activity of the postsqualene sterol pathway is decreased, and as a consequence, sterol

scavenging becomes the major mechanism for obtaining sterols (Andreasen & Stier, 1953). While S. cerevisiae is only able to take up exogenous sterols during anaerobic growth, some filamentous fungi such as Aspergillus fumigatus are able to take up sterols under aerobic conditions (Xiong et al., 2005). The molecular mechanisms behind aerobic sterol exclusion have not been elucidated, but heme has been implicated in the process. Cells are able to sense oxygen availability through Bioactive Compound Library the levels

of heme, which is produced in an oxygen-dependent mechanism. Heme stimulates transcription through the Hap1 transcriptional activator, and both heme and Hap1 are involved in aerobic ergosterol biosynthesis. Hap1 is responsible for aerobic induction and anaerobic repression of ROX1 (Ushinsky & Keng, 1994), a well-known repressor of hypoxic genes, which is activated upon expression of Hap1 in a heme-dependent mechanism (Keng, 1992). Many genes involved in the later steps of ergosterol biosynthesis require molecular oxygen for catalysis, and as a result, these enzymes are downregulated as the supply of oxygen declines. Likewise, because heme production is dependent on the supply of oxygen, heme-mediated Rox1 repression of hypoxic genes declines as oxygen levels decrease, resulting in an increased expression of nearly all GNAT2 Rox1 repressed genes (Kwast et al., 1997). The upregulation of hypoxic genes and decreased activity of

ergosterol biosynthetic genes results in exogenous sterol uptake. Many genes involved in cholesterol biosynthesis have homologs in ergosterol biosynthesis, and while many of these have been identified within the P. carinii genome, P. carinii does not appear to encode all of the genes necessary to synthesize cholesterol through a de novo pathway (e.g. C-5 desaturase). Thus, it is unlikely that P. carinii is able to synthesize cholesterol, and most, if not all, of the cholesterol found within the membranes of P. carinii was scavenged from host cells by P. carinii. The ability of P. carinii to scavenge lipids was confirmed after incubation of P. carinii with the fluorescent fatty acid analog Bodipy-C12. Fluorescent microscopy and fluorimetry indicated that P. carinii readily scavenged Bodipy-C12 from the medium and incorporated the fatty acid uniformly in all morphological forms of P. carinii (Furlong et al., 1997). Uptake of Bodipy-C12 by P.

albicans strain (Asai et al, 1999) Several enzymes of the posts

albicans strain (Asai et al., 1999). Several enzymes of the postsqualene ergosterol biosynthetic pathway require molecular oxygen, making ergosterol biosynthesis an oxygen-dependent process. When grown under aerobic conditions, S. cerevisiae is PLX-4720 nmr able to synthesize sterols, and is unable to acquire exogenous sterols, a phenomenon known as aerobic sterol exclusion (Andreasen & Stier, 1953). Under anaerobic conditions, the activity of the postsqualene sterol pathway is decreased, and as a consequence, sterol

scavenging becomes the major mechanism for obtaining sterols (Andreasen & Stier, 1953). While S. cerevisiae is only able to take up exogenous sterols during anaerobic growth, some filamentous fungi such as Aspergillus fumigatus are able to take up sterols under aerobic conditions (Xiong et al., 2005). The molecular mechanisms behind aerobic sterol exclusion have not been elucidated, but heme has been implicated in the process. Cells are able to sense oxygen availability through PD-0332991 cell line the levels

of heme, which is produced in an oxygen-dependent mechanism. Heme stimulates transcription through the Hap1 transcriptional activator, and both heme and Hap1 are involved in aerobic ergosterol biosynthesis. Hap1 is responsible for aerobic induction and anaerobic repression of ROX1 (Ushinsky & Keng, 1994), a well-known repressor of hypoxic genes, which is activated upon expression of Hap1 in a heme-dependent mechanism (Keng, 1992). Many genes involved in the later steps of ergosterol biosynthesis require molecular oxygen for catalysis, and as a result, these enzymes are downregulated as the supply of oxygen declines. Likewise, because heme production is dependent on the supply of oxygen, heme-mediated Rox1 repression of hypoxic genes declines as oxygen levels decrease, resulting in an increased expression of nearly all Olopatadine Rox1 repressed genes (Kwast et al., 1997). The upregulation of hypoxic genes and decreased activity of

ergosterol biosynthetic genes results in exogenous sterol uptake. Many genes involved in cholesterol biosynthesis have homologs in ergosterol biosynthesis, and while many of these have been identified within the P. carinii genome, P. carinii does not appear to encode all of the genes necessary to synthesize cholesterol through a de novo pathway (e.g. C-5 desaturase). Thus, it is unlikely that P. carinii is able to synthesize cholesterol, and most, if not all, of the cholesterol found within the membranes of P. carinii was scavenged from host cells by P. carinii. The ability of P. carinii to scavenge lipids was confirmed after incubation of P. carinii with the fluorescent fatty acid analog Bodipy-C12. Fluorescent microscopy and fluorimetry indicated that P. carinii readily scavenged Bodipy-C12 from the medium and incorporated the fatty acid uniformly in all morphological forms of P. carinii (Furlong et al., 1997). Uptake of Bodipy-C12 by P.